The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B2-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-.ALPHA. and Angiotensin II

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  • Yayama Katsutoshi
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
  • Hiyoshi Hiromi
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
  • Sugiyama Kaori
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University
  • Okamoto Hiroshi
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kobe Gakuin University

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  • The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B2-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-α and Angiotensin 2
  • Lipopolysaccharide Induced Up Regulation of Bradykinin B2 Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor アルファ and Angiotensin 2

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Our present study aimed to characterize the effects of lipopolysaccharide (LPS) on the expression of the bradykinin B2-receptor in the mouse heart, which may have a role in cardiac depression during sepsis. We found that LPS induced the up-regulation of B2-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Like LPS, tumor necrosis factor-α (TNF-α) but not interleukin (IL)-1-β, IL-6 or endothelin-1 stimulated B2-receptor expression in cultured myocytes. The effect of LPS on the expression of B2-receptor mRNA was also mimicked in cardiac myocytes by Ang II via Ang II type 1 (AT1-) receptor. Losartan, an AT1-receptor antagonist, inhibited about 50% of the LPS-induced up-regulation of B2-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Furthermore, the up-regulation of B2-receptor mRNA by either LPS or Ang II in cultured myocytes was abolished by anti-TNF-α antibody. These results suggest that the up-regulation of cardiac B2-receptor expression by LPS is mediated through TNF-α, which is produced in the myocardium by two different mechanisms in an AT1-receptor-dependent and independent manners, implying the role of the cardiac kallikrein-kinin system in the development of cardiac dysfunction during sepsis.

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